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HEMATOLOGY > Iron in HEALTH and DISEASE > Flashcards

Iron in HEALTH and DISEASE Flashcards

1
Q

Where is iron present?

A
  • Hb
  • Myoglobin
  • enzymes (cytochromes)
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2
Q

Why is iron dangerous?

A

chemical reactivity
(may cause Oxidative stress and free radical prdn)

—-should be transported, stored SAFELY

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3
Q

Can the body excrete iron?

A

NO

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4
Q

Where is MAJORITY of the body’s iron found?

A

In the haem

- Fe2+ ion sits in PROPHYRIN ring

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5
Q

How much iron is lost every day?

A

1 mg

loss d.t loss of cells –bleeding, mucosal cells

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6
Q

How much serum iron at any given time?

A

4 mg

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7
Q

Where is iron absorbed?

A
  • in DUODENUM

- —by duodenal mucosa

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8
Q

Which iron is readily absorbed?

A
  • HAEM-IRON
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9
Q

What enhances iron absorption?

A
  • ascorbic acid (reduces IRON to FE2+)

- alcohol

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10
Q

what inhibits iron absorption?

A
  • Tannins (TEA)
  • pHYTATES (CEREALS/ BRAN, NUTS AND SEEDS)
  • calcium (dairy products
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11
Q

WHat is involved in IRON absorption?

A
  • duodenal cytochrome B in the luminal surface (converts FERRIC 3+ iron to FERROUS iron)
  • DMT-1 transports ferrous iron INTO the duodenal enterocyte
  • Ferroportin (exports iron FROM the enterocyte—to transferin for transport)
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12
Q

What regulates iron absorption?

A

HEPCIDIN (produced in the liver)

—-incr. in response to INCR. IRON load and inflammation (malignancy)

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13
Q

What is MOA of hepcidin>

A
  • BINDS to ferroportin and CAUSES its DEGEN.

- –so iron is TRAPPED in duodenal cells and macrophages

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14
Q

What occurs to hepcidin levels when iron is deficient?

A
  • DECREASES
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15
Q

How to assess iron status? (3 compartments)

A
  1. Functional Iron (Hb conc.)
  2. Transport iron/ IRON supply to tissues (% saturation of TRANSFERRIN)
  3. Storage iron (serum FERRITIN/ tissue biopsy- rare)
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16
Q

What is transferrin?

A
  • transports iron from DONOR tissues (macrophages/ intestinal and liver cells) to the tissues EXPRESSING transferrin receptors
  • —-ALLOWS the SAFE transport of iron
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17
Q

What tissue is rich in transferrin receptors?

A
  • erythroid marrow (cells )
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18
Q

What is transferrin saturation?

A
  • measures IRON SUPPLY

- —serum iron/ total iron binding capacity (to transferrin) x 100%

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19
Q

What occurs in iron overload?

A
  • transport system is compromised

- –transferrin saturation is 100%

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20
Q

What does transferrin saturation reflect?

A
  • the proportion of diferric transferrin

HIGH affinity for cellular transferrin receptors

21
Q

What does a small level of serum ferritin indicate?

A
  • indirect measure of STORAGE iron

- –reflects intracellular ferritin synthesis

22
Q

When may ferritin serum levels go up?

A
  • with INFECTION and malignancy

it’s an ACUTE phase protein

23
Q

When is it best to look at ferritin levels?

A
  • for IRON deficiency.
24
Q

What does it mean by negative iron balance?

A

losing iron more than you are absorbing

25
Q

What are the consequences of NEGATIVE iron balance?

A
  1. exhaustion of iron stores
  2. iron deficient erythropoiesis
    * FALLING MCV)
  3. Microcytic anaemia
  4. Epithelial changes (Skin/ koilonychia/ angular stomatitis)
26
Q

What does hypochromic and microcytic anaemia indicte?

A

DEFICIENT Hb synthesis

27
Q

What 2 parameters to CONFIRM dx of iron deficiency>

A
  • Decr. Hb iron

- Reduced STORAGE iron (FERRITIN)

28
Q

What causes iron def.?

A
  • more likely women and children
  • vegetarian
  • too much bleeding
  • not absorbing enough (CELIAC disease)
29
Q

What are chronic causes of blood loss?

A
  1. menorrhagia
  2. GI (tumors/ ulcer/ NSAIDs/ parasitic infection)
  3. Hematuria
30
Q

What is meant by OCCULT blood loss?

A
  • GI blood loss of 8-10 ml per day (tsp)–4-5 mg of iRON

- —–MAX iron absorption is 4-5mg; negative iron balance may occur

31
Q

What is iron malutilisation?

A
  • anaemia of chronic disease
32
Q

Where is iron malutilisation commonly seen?

A

in hospitalized pts

33
Q

Why is iron def. seen in chronic disease pts?

A

d.t INFLAMMATORY macrophage IRON block —- Body’s reaction in making iron LESS available to the pathogen

34
Q

How does the inflammatory rxn result in IRON block?

A

Increased transcription of ferritin mRNA stimulated by inflammatory cytokines so ferritin synthesis increased
Increased plasma hepcidin blocks ferroportin-mediated release of iron
Results in impaired iron supply to marrow erythroblasts and eventually hypochromic red cells

35
Q

What occurs in Hereditary hemochromatosis?

A
  • mutation in HFE gene
  • —–decr. SYNTHESIS of HEPCIDIN
  • —-incr. iron absorption —-eventual iron accumulation and RISK of END-ORGAN damage.
36
Q

How does hereditary hemochromatosis present as?

A
  • fatigue
  • JOINT pain
  • IMPOTENCE
  • arthritis
  • CIRRHOSIS
  • DIABETES
  • cardiomyopathy
37
Q

How to dx Hereditary hemochromatosis?

A
  • transferin sat. >50%

- —incr. iron stores (serum ferritin >300in men and >200microgrma/l in pre-menopausal women)

38
Q

How to confirm dx of HHC?

A

0 LIVER biopsy

—-FIBROSCAN available to assess cirrhosis

39
Q

How to TREAT Hereditary hemochromatosis?

A 
WEEKLY VENESECTION (450-500ml) 
----intial aim to EXHAUST iron stores (<20 mcg/L ferritin) ---maintain at 50 mcg/L after
40
Q

chance of a first degree relative having hereditary hemochromatosis?

A

First degree relative of cases (esp. in SIBLINGS) - 1 in 4 chance !
—-kids WAIT until they are adults; for informed consent

41
Q

Is haemochromatosis asymptomatic?

A

YES until irreversible organ damage OCCURS

42
Q

What are the sources of iron-loading anaemias?

A
  • repeated red cell transfusions

- excessive IRON absorption related over erythropoiesis

43
Q

What disorders cause iron loading anemias?

A

(anaemia in the presence of HIGH serum ferritin/ transferrin)
- massive ineffective erythropoiesis (Thalassaemia and Sideroblastic anaemias)

  • refractory hypoplastic anaemias (red cell APLASIA and MYELODYSPLASIA)
44
Q

What refractory hypoplastic anaemias cause iron-loading anaemias?

A

red cell aplasia

myelodysplasia

45
Q

Explain the consequence of iron loading.

A

red cell transfusion and incr. iron absorption–> IRON OVERLOAD–> DAMAGE TO LIVER, HEART AND ENDOCRINE glands

46
Q

How to treat IIary iron overload?

A

—-IRON chelating agents (DESFERROIOXAMINE–S/c or Iv)

  • –desferipone
  • -deferasirox
47
Q

Why is venesection not ideal in IIaryiron overload?

A

— not ideal to perform on an already ANEMIC pt

48
Q

What is seen in Sideroblastic anaemia?

A
  • EXCESS iron build up in MITOCHONDRIA (failure to incorp/ iron in to haem)
49
Q

Why is iron essential?

A
  • oxygen transport

- electron transport (mitochondrial prodn of ATP)

HEMATOLOGY (20 decks)

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